Long noncoding RNA VPS9D1-AS1 promotes esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway

被引:16
作者
Ma, Liang [1 ]
Yan, Wenyue [1 ]
Sun, Xingwei [2 ]
Chen, Ping [1 ]
机构
[1] Nanjing Univ, Yancheng Hosp 1, Peoples Hosp Yancheng 1, Dept Oncol,Affiliated Hosp,Med Sch, Yulong West Rd 166, Yancheng 224001, Jiangsu, Peoples R China
[2] Soochow Univ, Dept Intervent, Affiliated Hosp 2, Sanxiang Rd 1055, Suzhou 215004, Jiangsu, Peoples R China
关键词
VPS9D1-AS1; long non-coding RNA; prognosis; Wnt/beta-catenin; esophageal squamous cell carcinoma; POOR-PROGNOSIS; CANCER; PROLIFERATION; INVASION; LNCRNA; STATISTICS; MIGRATION;
D O I
10.7150/jca.54556
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The VPS9D1 antisense RNA1 (VPS9D1-AS1, lncRNA MYU) can act as an oncogene or an antioncogene in different malignancies. In the present study, we demonstrated that VPS9D1-AS1 is significantly upregulated in esophageal squamous cell carcinoma (ESCC) and assessed its biological function and clinical prognosis. RNA-sequencing was conducted in four pairs of ESCC tissues and normal adjacent tissues (NATs). Compared with controls, lncRNA VPS9D1-AS1 was highly expressed in ESCC tissues, cell lines and plasma. VPS9D1-AS1 upregulation significantly correlated with the histopathological grade and clinical stage of ESCC. Analyses revealed poor prognosis in ESCC patients with high VPS9D1-AS1 expression. VPS9D1-AS1 knockdown led to the inhibition of tumor proliferation, migration, and invasion in vivo and vitro. VPS9D1-AS1 silencing downregulated the Wnt/beta-catenin signaling pathways by acting on key proteins such as beta-catenin and c-Myc. However, the expressions of these proteins increased after the addition of pathway agonist CT99021. Therefore, taken together VPS9D1-AS1 is highly expressed in ESCC and its expression can lead to poor prognosis. In conclusion, this study suggested that VPS9D1-AS1 acts as a vital part in facilitating ESCC progression and can be a potential biomarker for the diagnosis of patients with ESCC.
引用
收藏
页码:6894 / 6904
页数:11
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